Veterinary Medicine Library

Description

White snakeroot is an erect, branched herb usually about 3 feet tall but varying from 1
to 5 feet. It has slender, round stems and branches bearing pointed, oval, oppositely
placed leaves. These leaves, 3 to 5 inches long and petioled, are sharply toothed on the
margins. Each leaf has 3 main veins that show prominently on the underside. The roots are
fibrous, coarse, and shallow.

Early growth

With flowers

In late summer, numerous small heads of minute white flowers appear at the top of the
stem and the ends of the branches. These flower heads, except that they are white, are
almost exactly like the flower heads of the familiar ageratum of gardens. Later the
flowers are replaced in the heads by small black seeds each with a crown of soft white
hairs.

Because the leaves of white snakeroot resemble those of the nettle, other plants with
nettle-like leaves are often mistaken for it. Two such plants are the nettle-leaved sage
and the nettle-leaved vervain. Even without flowers or fruit, these plants can be easily
distinguished from white snakeroot. The nettle-leaved sage, a rare plant in some southern
Illinois counties, has square stems; white snakeroot stems are round. The nettle-leaved
vervain, a common weed throughout Illinois, has lance-shaped leaves; white snakeroot
leaves are broad at the base but narrow quickly in a wedge-shaped part to the petiole.

Distribution

White snakeroot is found in woods of all types and along streams in wooded pastures
throughout the Midwest. It persists after woods are cut, and often may be found many years
after the land has been cleared, although usually in such areas it occurs only as
scattered unthrifty plants. In prairie regions, it is not often found except in the woods
bordering streams.

Conditions of poisoning

An animal may die from eating either a large amount of white snakeroot at one time or
small amounts over a long period. The eating of small quantities more or less continuously
gives rise to the animal disease known as trembles. It is also the cause of the well-known
and much-feared milk sickness of man -- a disease that is contracted from drinking milk or
eating milk products from poisoned cows. Milk sickness claimed thousands of lives in the
early 1800s, perhaps the most well-known victim being Abraham Lincoln's mother. Nursing
calves and lambs may die from their mothers' milk contaminated with snakeroot even though
the mother animals show no signs of poisoning. Cattle, horses, and sheep are the animals
most often poisoned.

Control

During the dry period of late summer, animals should not be pastured in woods or fields
where there is white snakeroot. If the pasture is known to be infested, animals should be
moved out of it within the first few days of July and should not be returned to it until
the following year.

Eradication of white snakeroot is not easy. Chemical weed-killers cannot be used
satisfactorily, because they endanger trees and other plants of the pasture. The best way
to reduce the number of the plants is to pull them out by the roots and burn them; the
best time to do this is in September, when the plants are more easily identified by their
white blossoms. If the plants are pulled after a hard rain while the ground is soft, the
shallow roots come out readily.

Toxic principle

The apparent toxic principle in white snakeroot has been given the trivial name
tremetol. It has been described as a fat-soluble, high molecular weight alcohol.

Crude tremetol, was later shown to be separable into a toxic ketone fraction (61%)
(tested in goldfish) and a nontoxic sterol fraction (39%). The ketone fraction was later
separated into tremetone, dihydrotremetone, and hydroxytremetone. These may all be
components of a fragile tremetol molecule.

Clinical signs

White snakeroot can endanger the lives of persons and animals other than those that
have actually eaten the plant.

In cattle and sheep:

Although animals that have fed on white snakeroot may be listless and somewhat inactive
at first, the first noticeable manifestations of poisoning are loss of weight and
trembling following exercise. Trembling is especially marked in the muzzle and legs. As
poisoning progresses, cattle lose appetite, become constipated, lose weight, and gradually
become weaker until they are not able to stand. Additional signs may include a peculiar
odor to the breath and urine, excessive salivation, and quickened, difficult breathing.
Later, complete relaxation without tremors and coma are seen, with death following in 2-10
days.

The clinical signs that are exhibited by poisoned sheep are similar to those shown by
cattle. Death may occur in a few days or may be delayed.

The onset of clinical signs in white snakeroot poisoned horses is within 2 days to 3
weeks after initial ingestion (usually after at least several days of ingestion). The
major effects are related to congestive heart failure. Tremors are inconsistently observed
in horses with white snakeroot poisoning. Horses may stand with legs wide apart. Sweating
may be evident especially between rear legs, and stumbling in the rear legs may be noted
when horses are turned. Severe depression, bloody urine, and/or choking may also occur.
Sometimes swelling is present in the lower neck area, near the thoracic inlet. They may
exhibit a jugular pulse and a rapid heart rate. Changes in electrocardiogram include
increased heart rate, ST elevation, and variable QRS complexes, and ventricular premature
beats. Cardiac arrhythmias are often present.

In guinea pigs:

The refusal to eat by the animal is the first sign, followed by listlessnss and
crouching with half-closed eyes. The hair becomes rough. Muscular tremors may not be
noticeable, but complete lack of muscular coordination and stupor precede death. (White
snakeroot poisoning, by R. Graham and V.M. Michael. Circular #436, University of
Illinois College of Agriculture,1935.)